More Annoyance

I try to eat and drink healthy. I try to avoid premade 'chemical' food and use whole ingredients, meaning real, unprocessed food. In the mornings it may not be wise to get between me and my first cup of coffee. Later in the day, I like my herbal tea for its flavors and lack of caffeine anytime after 10 am. My husband makes fun of all the different kinds of herbal teas I have. I just like to be able to choose which one I am in the mood for.

I also subscribe to tips from WebMD to help keep me up on how to be healthier, what to do or eat or what not to. Usually I find this helpful.

But not yesterday.

I got an email on good and bad herbal teas. I know there are some herbs in teas that can interact with medications. I made a point of reading the information each of the herbal teas and stopped at Rooibos because I don't know much about it and I know I have some. This is what I learned:

"It comes from a plant native to South Africa, and the drink there is called redbush tea. It’s caffeine-free and is often touted for its antioxidants. Some researchers believe, based on studies done on animals, that this herb may boost the immune system and help prevent cancer. They are also looking into whether it can benefit your heart and fight diabetes. Check with your doctor before you use it if you have a hormone-sensitive cancer or you’re on chemotherapy."

Did you read that last sentence? Hormone sensitive cancer? That's me. Now I have to sort through all my teas to pull out any with rooibos. 

This just annoys me. One more thing that just aggravates me. Can't I just be a person who had cancer instead of having to check labels on herbal teas, and everything else for soy? Annoyance, annoyance, annoyance.

New Breast Cancer Research Found A Factor that Doubles Death Risk

Isn't that a warm fuzzy feeling? Now I want to ask my oncologist if I have this factor. But first let me see if I can explain it. This is the precis:

"Researchers at Karolinska Institutet in Sweden have discovered that the risk of death from breast cancer is twice as high for patients with high heterogeneity of the estrogen receptor within the same tumour as compared to patients with low heterogeneity. The study, which is published in The Journal of the National Cancer Institute, also shows that the higher risk of death over a span of 25 years is independent of other known tumour markers and also holds true for Luminal A breast cancer, a subtype with a generally good prognosis."

Apparently Luminal A breast cancer is a subtype of hormone receptor positive that usually is a good thing. But if your hormone receptor status changes when you develop a metastases or even with in your first tumor (which sometimes happens). 

"Why this is the case, however, is not known, but a possible explanation is that there are tumour cells in one and the same tumour with varying degrees of expression of the estrogen receptor. This is known as intra-tumour heterogeneity."

But some recent research found that patients with high heterogeneity and Luminal A breast cancer, regardless of previous treatment, were found to have double the death risk. 

"Our study shows that patients with high intra-tumour heterogeneity of the estrogen receptor were twice as likely to die up to 25-years after their diagnoses as compared to patients with low heterogeneity," says Linda Lindström, researcher at the Department of Biosciences and Nutrition, Karolinska Institutet. "And this was independent of whether or not they'd received tamoxifen and of other known tumour markers."

The researchers also discovered that the greater risk of death for patients with high intra-tumour heterogeneity also applied to patients with Luminal A breast cancer, a subtype of estrogen-receptor-positive breast cancer that is considered to have a good prognosis."

So what does this all  mean to the average bear breast cancer patient? Me, I'm going to add this to the growing list of things to ask my oncologist. I don't know if I was ever tested to find out about heterogeneity or Luminal A and if I can be now. But I want to find out.

This is a classic case of new research on cancer finding more differences in the different types of cancer. As we have learned, cancer is not one disease but hundreds, or thousands of different diseases. Scientists are slowly unraveling them one step at a time. Sometimes panicking us patients, and sometimes making us feel a little bit better. But the process is way longer than I want.

That Er+/Pr+ Thing

So I haven always known (well since my diagnosis - before my diagnosis what I knew about breast cancer wouldn't fill a post-it) that have a hormone receptor positive breast cancer had a lot of impact on your treatment protocol. But I didn't know that much about how that worked.

Now I am learning more. In the past, estrogen was considered to be the indicator of breast cancer diagnosis. When estrogen was detector at a biopsy, it was considered an indicator of breast cancer. Now it has been determined that progesterone has a big impact as well.

"Previous studies have demonstrated that estrogen receptors react to the primary female sex hormone, estradiol, by activating genes that nudge cancer cells into growing and replicating. The cells divide faster and live longer, which results in a more advanced state, Greene explained.

The study concluded that when progesterone or progestin is added, an entirely new set of binding sites opens up, allowing the estrogen receptor to work in conjunction with progesterone receptors. The process stops cell reproduction and survival and "our data further suggests that, despite the historical bias toward the effects of estrogen on the estrogen receptor," Greene said. "It’s the progesterone receptor that dominantly controls estrogen activity when both receptors are present and activated.""

Well whoop de doo. This sounds all kinds of complicated. But I think its important.

"During the study, Greene and his colleague Haral Singhal inhibited the activity of both estrogen and progesterone receptors in three groups of mice by treating them with either the estrogen receptor antagonist tamoxifen, an experimental progesterone receptor antagonist called CDB4124, or a placebo. Predictably, tumors in untreated mice grew quickly. Tamoxifen halted tumor growth, but did not shrink them, while CDB4124 had a more complicated effect: It caused the tumors to shrink at first, but after 35 days, they began growing again and ended up 50 percent larger than their original size. A combination of the two antagonists seemed to be the golden ticket: tumors showed “virtually full regression,” according to Singhal.

“These findings,” the study reads, “emphasize the clinical value of assessing both progesterone receptor and estrogen receptor expression in breast cancer samples.”"

Sorry its a bit technical but this is a big change in looking at breast cancer treatment options.

The way of the future

My non-medical opinion of cancer treatment is that there are a lot of assumptions built it. If you have a tumor,they should take it out. If they think you need chemotherapy, they guess at the dose based on your body weight. If you need radiation, they try to hit only where the tumor was, this is a change from hitting the entire area of the body. They assume you will respond as well as everyone else who had the same treatment protocol but realize that not everyone does and they don't necessarily understand why. It is realized that many cancer patients are either under treated or over treated because they simply don't understand enough about cancer.  And often the treatment is almost as bad as the disease - it causes significant short (hair loss, nausea, etc.) and long term side effects (future cancers from radiation and chemotherapy, heart damage).

Cancer treatment is often only treating the symptoms. Surgery excises the tumor and the clump of cells. They hope chemotherapy will zap any remaining cancer cells in your body - but my non medical brain asks if chemotherapy zaps all cancer cells, why are there so many kinds of chemo if they zap all cancer cells? I feel that this goes back to the all cancers are the same theory that was disproved generations ago. One treatment does not fit all. Radiation tries to zap the cancer cells in a certain area - where they think they are. But it also damages the healthy cells and causes all kinds of burning. Some systemic treatments like Tamoxifen or aromatase inhibitors work for some women and not for others and are trying to make your body less attractive to hormone receptor cancer cells.

But none of these treatment focus on what I call the key questions:

- Where did these cancer cells come from? Why did they start mutating in the first place?
- Why was this part of the body more attractive to the cancer cells than others?
- What is the underlying cause of all of this?
 
When I heard Dr Love talk on Friday and she talked about the importance of the type of cancer not just its location, I was intrigued to say the least. I have also heard many times of the trend to personalized medicine. But now the next step is beginning to expand on these areas and actually take concrete steps to make changes.

Brigham and Women's Hospital and Dana-Farber Cancer Institute have launched a massive study to test cancer patients' tumors for hundreds of genetic aberrations. The goal is to obtain a better understanding of the underpinnings of cancer and how to tailor patient's treatments.  They want to have 10,000 patients each year to include in their study.

There is another program at Mass General since 2009 where they have been scanning the genes of 50-60 patients each week of their tumor tissue and have identified 160 genes and 15mutations. Their goal is to help guide treatment or to pave the way for new clinical trials. MD Anderson is moving toward a broad genetic analysis of all cancer patient's tumors.

There are two issues here. Dr Susan Love wasn't talking about  genetic markers but more of the type of tumor characteristics - hormone receptors, Her2/nu status, etc. However as cancer cells have damaged DNA, their genetic sequencing grows in importance.

I think this is the way of the future and how we will look at cancer as we move forward in both a way to find their cause and to find a cure.